A narrative review of Catamenial dermatology: A glimpse into the menstrual symphony

Vijayasankar Palaniappan; Hima Gopinath; Aravind Baskar Murthy; Ankan Gupta; Kaliaperumal Karthikeyan

doi:10.25259/IJDVL_926_2024

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Review Article

ARTICLE IN PRESS

doi:

10.25259/IJDVL_926_2024

A narrative review of Catamenial dermatology: A glimpse into the menstrual symphony

Vijayasankar Palaniappan^1,, Hima Gopinath², Aravind Baskar Murthy³, Ankan Gupta⁴, Kaliaperumal Karthikeyan⁵

1Department of Dermatology Venereology and Leprosy, Sri Manakula Vinayagar Medical College and Hospital, Pondicherry, India

2Department of Dermatology, All India Institute of Medical Sciences Mangalagiri, Mangalagiri, India

3Department of Dermatology, SRM Medical College and Hospital, Chengalpet, India

4Department of Dermatology, Christian Medical College, Vellore, India

5Dermatology, Venereology, and Leprosy, Sri Manakula Vinayagar Medical College & Hospital, Pondicherry, India

Corresponding author: Dr. Vijayasankar Palaniappan, Department of Dermatology Venereology and Leprosy, Sri Manakula Vinayagar Medical College and Hospital, Puducherry, India. vijayasankarpalaniappan@gmail.com

Received: 2024-06-24, Accepted: 2025-04-15, Epub ahead of print: 2025-07-04,

Licence

This is an open-access article distributed under the terms of the Creative Commons Attribution-Non Commercial-Share Alike 4.0 License, which allows others to remix, transform, and build upon the work non-commercially, as long as the author is credited and the new creations are licensed under the identical terms.

How to cite this article: Palaniappan V, Gopinath H, Murthy AB, Gupta A, Karthikeyan K. A narrative review of Catamenial dermatology: A glimpse into the menstrual symphony. Indian J Dermatol Venereol Leprol. doi: 10.25259/IJDVL_926_2024

Abstract

The menstrual cycle induces a wide range of physiological changes in the skin and its appendages, often overlooked in dermatologic practice. Catamenial dermatoses, influenced by hormonal fluctuations, present with cyclical skin manifestations. This review explores the underrecognized intersection between menstruation and dermatology, highlighting changes across menstrual phases such as variations in hydration, lipid levels, pigmentation, hair and nail growth, and sweat gland activity. Autoimmune progesterone dermatitis and estrogen dermatitis are key examples of hormone-induced skin responses. These conditions have complex pathogenesis, variable clinical features, and present diagnostic challenges. Treatment options include hormonal suppression and newer therapies such as omalizumab. The review also examines the link between menstruation and increased susceptibility to infections, as well as the flare of preexisting dermatoses. Conditions such as acne, psoriasis, and atopic dermatitis may worsen in relation to hormonal shifts. Understanding the cyclical responses of skin to endogenous hormones can help clinicians better identify and manage hormone-responsive dermatoses, ultimately improving diagnosis and patient care.

Keywords

Catamenial

menstruation

progesterone hypersensitivity

autoimmune progesterone dermatitis

menstrual toxic shock syndrome

cutaneous endometriosis.

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Introduction

The menstrual cycle orchestrates a silent symphony within a woman’s body, influencing various physiological systems, including the skin and appendages. The term “catamenial” is derived from the Greek word “katamenia,” which refers to the monthly menstrual flow. Catamenial dermatoses, also known as menstrual-related skin disorders, represent a unique and often under-recognised category of dermatological conditions that are influenced by the hormonal fluctuations of the menstrual cycle. These conditions can significantly impact the quality of life for affected individuals, often presenting with cyclical exacerbations that coincide with specific phases of the menstrual cycle.^1-4 Despite their prevalence, catamenial dermatoses are frequently overlooked or misdiagnosed, leading to prolonged patient discomfort and distress. This narrative review aims to provide a comprehensive overview of the current knowledge of catamenial dermatoses, including their pathophysiological mechanisms, clinical manifestations, diagnostic challenges, and management strategies.

We conducted a comprehensive English literature search across multiple databases, including PubMed, SCOPUS, EMBASE, MEDLINE, and Cochrane. Using various Boolean operators, we searched with keywords such as ‘menstrual cycle,’ ‘menses,’ ‘skin,’ ‘catamenial dermatoses,’ ‘catamenial dermatology,’ ‘cyclic dermatoses,’ ‘hormone,’ ‘estrogen,’ and ‘progesterone’ individually and in combinations. Our search yielded 68 relevant articles. Additionally, we analysed the references of these articles for further relevant content.

Hormonal changes in the menstrual cycle

Menstruation marks the start of the cycle (Day 1). During the follicular phase (typically Days 7–14), the ovaries secrete oestrogen, with oestradiol, the most potent form, peaking one day before ovulation. The luteal phase begins after ovulation, around Day 14, and lasts until Day 28. In this phase, the corpus luteum develops, producing progesterone, while oestradiol levels rise again about five days post-ovulation. As the luteal phase concludes, declining levels of oestrogen and progesterone trigger the onset of menstruation.⁵

Circulating sex hormones, namely, oestrogens, progesterone, and androgens, play a key role in skin homeostasis. Oestrogen receptors are widely distributed in the epidermis and dermis, with Estrogen Receptor-β predominantly present in basal keratinocytes, sebocytes, and eccrine sweat glands and ER-α in the sebocytes. In contrast, progesterone receptors are mainly found in the nuclei of the keratinocytes and sebocytes. Androgen receptors are seen in keratinocytes, about 10% of dermal fibroblasts, sebaceous gland basal cells, sebocytes, and the hair follicle dermal layer, though rare in eccrine sweat glands. This distribution suggests that menstrual cycle–related hormonal changes may significantly influence skin cell activity and contribute to cutaneous disease.^6,7 Table 1 outlines the normal effects of various hormones on the skin and its adnexal structures.^5-11

Table 1: Effect of oestrogen, progesterone, and androgens on the skin and adnexal structures

Effect of oestrogen

Stimulation of melanogenesis

Increase mitotic activity in the epidermis

Increase skin thickness

Reduce sebum (high levels)

Decreased collagen breakdown and increased collagen production

Increased water-binding capacity and increased fluid retention

Immunomodulation

Increased vasodilation, increased elasticity

Macrophage polarisation M1 to M2

Reduction in inflammation and oxidative stress

Reduction of proteolysis in the extracellular matrix

Increase in granulation, angiogenesis, re-epithelialisation, and wound contraction

Effect of progesterone

Increases sebum production and influences hair follicle sensitivity to androgens.

Stimulates melanin synthesis, leading to increased skin pigmentation.

Induces peripheral vasodilation, contributing to increased skin temperature and vascular permeability in the vulva/vagina.

Reduces epidermal water loss and stimulates vaginal epithelial cell proliferation.

Modulates immune responses by suppressing Th1 and increasing Th2 cytokine production.

Increases production of thick cervical mucus

Effect of androgens

Increases sebocyte proliferation, boosting sebum production via androgen receptor activation.

Prolongs the anagen phase of hair growth in androgen-sensitive areas, promoting terminal hair development.

Stimulates fibroblast collagen synthesis, increasing dermal thickness.

Enhances angiogenesis, potentially promoting wound re-epithelialization.

Modulates cutaneous cytokine expression, influencing the pathogenesis of inflammatory dermatoses.

May suppress cell-mediated immunity locally in the skin, potentially increasing susceptibility to certain skin infections.

Alters the Th1/Th2 balance in the skin, contributing to the modulation of inflammatory conditions.

Stimulates apocrine gland secretion, contributing to body odour and potentially exacerbating hidradenitis suppurativa.

Induces hair follicle miniaturisation in the scalp via dihydrotestosterone (DHT), leading to androgenetic alopecia.

Modulates the production of antimicrobial peptides by sebaceous glands, influencing skin microbiome dynamics.

Physiological effects on skin and appendages

In skin

Fluctuating hormone levels cause numerous physiological changes in the skin. Skin thickness, subcutaneous fat, and elasticity vary throughout the menstrual cycle. However, the data is limited, and the mechanisms are unclear.³ Increased transepidermal water loss, surface lipids, and microflora have been reported in the luteal phase. The skin is drier during menses and the early proliferative phase. A study found that women were very susceptible to ultraviolet light during days 20 to 28 of the menstrual cycle.⁴

Sweat glands

Internal body temperature increases in the luteal phase, but conflicting or insufficient data exist on sweat rate and mean skin temperature changes during the menstrual cycle.¹²

Hair

“Bad hair days” (BHD) are when many women complain that their hair is periodically unmanageable. Interestingly, a study found that though BHDs occurred throughout the menstrual cycle, they were more common during menstruation.¹³

Nails

The nails grow faster in the premenstrual phase. Physiological Beau’s lines and transverse leukonychia may be seen with each menstrual cycle.¹⁴

Catamenial pigmentary changes

Sex steroids can regulate pigmentation, but the mechanisms are not clear. Oestrogen increases the activity of melanogenic enzymes through the melanocyte oestrogen receptors. Androgens also regulate pigmentation through their effects on cyclic Adenosine Monophosphate (cAMP).¹⁵ Increased pigmentation has been reported in the luteal phase in small studies, in the peri-ocular region with questionnaires, and in the cheek and under-eye area based on colour reflectance.^16,17

Aberrant skin response to hormones

Autoimmune progesterone dermatitis

Autoimmune Progesterone Dermatitis (APD) was initially described in 1964.¹⁸ APD, now proposed to be renamed as progesterone hypersensitivity (PH) is an infrequent, cyclical, immunological disorder that afflicts women during the progesterone surge in the luteal phase.^19-21 Although the precise pathogenesis of this condition remains elusive, the primary mechanism involves exposure to endogenous or exogenous progesterone, provoking hypersensitivity reactions that culminate in the clinical manifestation of the disease. Progesterone, widely used in IVF and intracytoplasmic sperm injection cycles to enhance implantation and pregnancy rates, has been increasingly linked to dermatitis due to supraphysiological doses.¹⁹ In a prospective study of 200 IVF patients, Sood et al. found dermatological manifestations in 27%, with urticaria (13.5%) being the most common, followed by acneiform eruptions (3%). Notably, 96.3% of urticaria cases occurred in patients on progesterone.²² Pregnancy-associated APD can be triggered by endogenous progesterone from the corpus luteum and placenta. Symptoms may begin intrapartum, persist postpartum, or arise after childbirth. Paradoxically, preexisting APD may improve intrapartum due to auto-desensitisation from rising progesterone levels or a reduced maternal immune response.¹⁹ The classification of APD based on inciting factors has been mentioned in Table 2.²³

Table 2: Classification of APD^*

Classification	Inciting factor	Timing of symptoms
Endogenous	Pregnancy	Symptoms onset during pregnancy and may endure into the postpartum period
Endogenous	Menses	Symptoms preceding menstruation
Exogenous	Supplementary progestins for fertility enhancement or contraception	Onset occurs after exposure to exogenous progestins.
Mixed	Supplementary progestins for fertility enhancement or contraception	It begins after exposure to exogenous progestins but continues alongside premenstrual or pregnancy symptoms.

* Modified and adapted from Foer et al.²³

The disease onset reaches its peak in the third decade, although it can manifest at any point between menarche and menopause.¹⁹ The cutaneous lesions due to endogenous APD typically emerge 3-10 days preceding the onset of menstruation, coinciding with a surge in progesterone levels, and resolve a few days after menses begin. The diversity of symptoms is a distinguishing characteristic of APD. There is a noted propensity for symptoms to evolve within a single individual.^24,25 Clinically, it manifests as pruritus, eczema, papulovesicular eruption, maculopapular rash, urticaria, angioedema, stomatitis, erythema multiforme, folliculitis, fixed drug eruption, aphthous ulcers, purpura, erythema annular centrifugum, necrolytic migratory erythema, vulvovaginitis, and labial swelling^11,26-32 [Figures 1-3]. Systemically, it can induce asthma and severe anaphylaxis.³³

A patient of APD manifesting as erythema multiforme.

APD manifesting as fixed drug eruption during menstrual cycle.

A thorough clinical history and physical examination are often sufficient to diagnose APD. Skin prick and intracutaneous tests are deemed unreliable as diagnostic tools for immediate and delayed PH.^19,34 [Figure 4] This unreliability stems from the nature of progesterone as a steroid, which necessitates suspension in oil or ethanol as a diluent, thereby limiting the positive predictive value of test outcomes due to potential irritant-induced reactions from these diluents.³⁵ A study reported a staggering 90% rate of false-positive intracutaneous progesterone skin test responses.³⁶ Skin tests may produce late reactions, requiring prolonged surveillance for accurate assessment.³⁴ Since some authors consider APD an autoimmune disease, tests like the autologous serum test, used in autoimmune urticaria, have been applied in select cases.³⁵

Intradermal testing with progesterone (1:1 and 1:10) was positive.

Histological characteristics of APD lack specificity and depend on the morphology of the lesion, with superficial perivascular mixed inflammation being the most consistent pathological finding.³¹ There are no standardised in vivo or in vitro tests for APD diagnosis. Various case reports propose different testing methods for suspected cases.³⁴ Ghosh et al. have recently pioneered the development of an ELISA progesterone assay, marking a significant advancement in this area of research. This assay’s sensitivity, specificity, and positive and negative predictive values were 82%, 100%, 86%, and 100%, respectively, with the basophil mediator release assay results as the gold standard. The impending commercialisation of this assay promises clinicians access to a more dependable diagnostic tool for PH.³⁷ An alternative method proposed for assessing APD and associated T-cell activity in delayed-type hypersensitivity is the IFN-γ-release assay.³⁸

Treatment for APD is tailored to each patient and hinges on factors such as symptom severity and the individual’s fertility preferences.²³ For patients who are not pursuing pregnancy, managing or treating APD may involve suppressing ovulation to halt the secretion of endogenous progesterone. Ovulation can be suppressed with oral contraceptives, danazol, tamoxifen, and gonadotropin-releasing hormone agonists such as leuprolide and nafarelin.^20,23,32 In persistent symptoms, hysterectomy and bilateral oophorectomy may be considered as a last resort.²¹

In women who wish to conceive, oral corticosteroids combined with antihistamines can be given.³⁹ Desensitisation can be employed as a safe alternative for symptom control in patients who want to circumvent the potential adverse effects linked with the hormonal agents. ^27,33 Omalizumab could serve as a viable treatment option for individuals experiencing recurrent urticaria or anaphylaxis.^40,41

A Jamaican woman with recurrent Stevens-Johnson-type reactions, provisionally diagnosed with APD linked to prostaglandin release, showed a positive prick test for 0.01 mL of a PG-F2 analogue. After a hysterectomy for endometriosis-related complications, her symptoms resolved completely.⁴²

Oestrogen dermatitis

Oestrogen dermatitis is an uncommon cutaneous reaction to fluctuating endogenous oestrogen levels during the menstrual cycle. Initially, it was proposed by Shelly et al. in 1995 based on premenstrual exacerbations of skin lesions among seven women.^43-45 The underlying mechanisms of oestrogen dermatitis have yet to be fully elucidated. Clinically, it can present as generalised pruritus, papulovesicular, bullous, prurigo multiforme, urticarial, or eczematous lesions. The cutaneous lesions typically appear 14 days pre-menstrually and remit shortly after menstruation. A positive immediate or delayed reaction to intradermal oestrogen supports the diagnosis.^44,46 Therapeutic options for oestrogen dermatitis include oestrogen desensitisation, tamoxifen, leuprolide, omalizumab, and oophorectomy. Oestrogen-induced dermatitis, even resistant to oophorectomy, has demonstrated a favourable response to treatment with omalizumab.^44,46 A comparative overview of APD and oestrogen dermatitis has been mentioned in Table 3.^23,29,44,45 The menstrual cycle and the related conditions have been depicted in Figure 5.

Table 3: Difference between APD and oestrogen dermatitis

Aspect	APD	Oestrogen Dermatitis
Aetiology	Autoimmune reaction to endogenous or exogenous progesterone.	Hypersensitivity reaction to oestrogen, often during hormone therapy or changes in hormonal levels.
Trigger	Progesterone fluctuations, especially during the luteal phase of the menstrual cycle or hormone therapy involving progesterone.	Oestrogen fluctuations, particularly during hormone therapy or phases of the menstrual cycle with increased oestrogen levels.
Onset	3 – 10 days before the onset of menses	14 days prior to the onset of menses
Clinical presentation	Urticaria, eczema, erythema, papules, vesicles, and sometimes severe anaphylaxis. Lesions often appear in cyclical patterns.	Eczema, erythema, itching, and other dermatitis symptoms are often less cyclic but can be associated with periods of high oestrogen.
Diagnosis	History of cyclic symptoms, progesterone skin test, and serum progesterone levels. Symptom resolution after suppressing ovulation can confirm the diagnosis.	Clinical history, oestrogen skin test, and serum oestrogen levels. The correlation between symptoms and oestrogen peaks helps in the diagnosis.
Management	Avoidance of progesterone exposure, use of hormone therapy to suppress ovulation, corticosteroids, and antihistamines. In severe cases, oophorectomy might be considered.	Avoidance of oestrogen exposure, adjusting hormone therapy, corticosteroids, and antihistamines. In some cases, switching to non-estrogenic hormone therapy might be necessary.
Prognosis	It can be well-managed with appropriate hormonal and symptomatic treatment, though complete resolution can be challenging.	Generally manageable with adjustments to hormone therapy and symptomatic treatment. Prognosis varies with underlying conditions and response to therapy.

Menstrual cycle and conditions related to it.

Menstruation and sexually transmitted infections

Studies show that 50–66% of females have had sex during menstruation, while 4–43% engage in it regularly. Cyclic changes in the vaginal microbiome and immunity may weaken antimicrobial defences, especially in those not using hormonal contraceptives.⁴⁷ As HIV has been identified in menstrual secretions, intercourse during menses renders the male partner more susceptible to acquiring HIV.⁴⁸ Decrease in iron and complement function during menstrual flow may facilitate colonisation, invasion, and ascending infection by Neisseria gonorrhoeae.⁴⁹ The majority of disseminated gonococcal infections develop during or immediately after menstruation.⁵⁰

A cross-sectional study of 1200 women found an increased risk of bacterial vaginosis in women engaging in sexual intercourse during menses.⁵¹ A survey revealed a significant statistical association between intercourse during menses and self-reporting of sexually transmitted infections, such as HIV, Trichomonas vaginalis, bacterial vaginosis, syphilis, chancroid, genital herpes, condyloma acuminata, chlamydia, gonorrhoea, and hepatitis B.⁵² Herpes simplex may recur during pre-menstrual, menstrual, and immediate post-menstrual periods (‘herpes menstrualis’). Rarely, regular recurrences may be seen during pregnancy or after menopause.⁵³

Dermatoses exacerbated with menstruation

Several dermatoses are reported to be exacerbated peri-menstrually [Table 4].^7,50,54-77 Perimenstrual exacerbations of dermatological conditions primarily stem from fluctuations in sex hormones, notably oestrogen and progesterone, and their modulation of inflammatory pathways. Pre-menstrual acne flares occur due to multiple factors [Figure 6]. Elevated androgens and oestrogens in the follicular phase and around ovulation increase sebum production and skin lipids, promoting microflora growth. Consequently, low progesterone levels later in the menstrual cycle contribute to acne exacerbation.^56,57 Nearly half of atopic eczema patients experience a flare-up in the week before menstruation, which quickly improves once bleeding begins. Increased skin permeability during this time makes the skin more vulnerable to allergens and irritants, contributing to these pre-menstrual flares.^58,59

Table 4: Dermatoses that can exacerbate with menstrual cycles

Acne vulgaris

Anogenital pruritus

Aphthous ulceration

Atopic eczema

Autoimmune progesterone dermatitis

Autoimmune oestrogen dermatitis

Beau’s lines

Behcet’s syndrome

Bullous pemphigoid

Contact dermatitis

Cholestatic pruritus

Darier’s disease

Dermographism

Dermatitis herpetiformis

Erosive adenomatosis of nipple secretions

Erythema annular centrifugum

Erythema multiforme

Exercise-induced angioedema

Flushing of face

Gardner-Diamond Syndrome

Glomangiona

Glossodynia

Hand eczema

Hailey-Hailey disease

Hobnail haemangioma

Haemangioma

Hereditary angioedema

Herpes simplex

Hidradenitis suppurativa

Impetigo herpetiformis

Keratolytic winter erythema

Leukonychia

Lichen planus

Lupus erythematosus

Melasma

Neuroticism

Nevus of Ota fluctuation in the intensity of colour

Pemphigoid gestationis

Pompholyx

Psoriasis

Pyoderma gangrenosum

Raynaud phenomenon

Recurrent vulvovaginal candidiasis

Rosacea

Solitary fibrous tumour

Translucent periocular skin

Trichotillomania

Trimethylaminuria odour

TNF Receptor-Associated Periodic Syndrome (TRAPS)

Ulcerative stomatitis

Urticaria

Varicose veins cutaneous symptoms

A young women who experience premenstrual flare-up of acne vulgaris.

Hidradenitis suppurativa, though more closely associated with androgens, can experience perimenstrual exacerbations due to fluctuations in androgen sensitivity and progesterone’s impact on apocrine glands and inflammation.^60,61 A survey conducted among patients indicated that 204 out of 279 women (approximately 76.7%) observed a deterioration in symptoms related to hidradenitis suppurativa during menstruation.⁷⁸ Premenstrual hormonal shifts in psoriasis can disrupt immune responses and trigger a rebound of inflammatory cytokines, leading to flare-ups.^58,62 Premenstrual aphthous ulcers may stem from oestrogen-induced changes in mucosal immunity.⁶³

The depigmented macules in vitiligo have been reported to become pink or red in some young girls and women during menstruation (Punshi’s sign).⁷⁹ Exacerbation or recurrence of allergic contact dermatitis during the immediate premenstrual period is common. The follicular phase of the menstrual cycle reduces the sensitised state.⁸⁰ Hence, false-negative patch test readings are common during this phase.⁸¹ Catamenial exacerbations of skin neoplasms such as hobnail haemangioma, arteriovenous haemangioma, and solitary fibrous tumour have been reported.⁸²

Cutaneous endometriosis

Cutaneous endometriosis is a rare but well-recognised condition, accounting for 0.5%–1% of all endometriosis cases. Umbilical endometriosis, the most common type, was first described by Villar in 1886. It can be classified as primary or secondary based on surgical history. Primary umbilical endometriosis, or Villar’s nodule, occurs spontaneously in about 30% of cases, with an unclear aetiology. Secondary endometriosis typically follows abdominal or pelvic surgery due to lesion seeding.⁸³ Clinically, it presents as a firm subcutaneous papule or nodule, varying in colour from skin-coloured to blue or violaceous brown. Patients typically experience cyclical pain, swelling, and occasional bleeding corresponding with their menstrual cycle. Although the umbilicus is the most common site, other locations, such as episiotomy wounds, appendectomy scars, caesarean scars, groin, and arm, have also been documented.^84-90 Fine needle aspiration cytology should be avoided to prevent the seeding of endometriotic tissue in new areas.⁸⁹ Surgical excision with a safety margin of at least 1 cm from the skin lesion is diagnostic and therapeutic.⁹⁰ Hormonal agents that decrease the proliferation of endometrial tissue, such as oral contraceptives, danazol, and gonadotropin-releasing hormone agonists, may be considered. Recurrence following treatment and malignant transformation with histology indicative of endometrioid or clear cell carcinoma are potential complications associated with this condition.^83,85

Vicarious menstruation

Vicarious menstruation can be defined as extraneous bleeding originating from a location other than the uterine mucous membrane, coinciding with the expected onset of regular menstruation. Vicarious menstruation is a risk factor for haematohidrosis, a rare condition in which a patient sweats blood.^91,92

Dermatoses related to the use of menstrual hygiene products

Menstrual Toxic Shock Syndrome (mTSS) is a rare, life-threatening disease precipitated by superantigen-producing Staphylococcus aureus. Until the late 1970s, cotton was the primary absorbent material in tampons; however, manufacturers’ introduction of synthetic superabsorbent fibres led to significant Toxic shock syndrome toxin-1 (TSST-1) production.^54,93,94 The incidence of Toxic Shock Syndrome (TSS) reached its peak in the early 1980s, after which there was a decrease in menstrual TSS cases attributed to mandatory tampon labelling and enhanced patient education. Overall rates of TSS have remained relatively consistent since the late 1980s, currently ranging from 0.8 to 3.4 per 1,00,000 adults and 0.4 per 1,00,000 in children.^94,95-97

According to the US Centres for Disease Control and Prevention, TSS is considered menstrual-associated if onset occurs less than four days before the onset of menses. Table 5 mentions the Centre for Disease Control (CDC) case definition of TSS.⁹⁷ The development of mTSS involves a complex interplay between the use of intravaginal devices such as tampons, the pathogenicity of S. aureus, host immunity, immunological mechanisms, and alterations in the vaginal ecosystem during menstruation. Instances of TSS in adults unrelated to tampon usage have also been documented, including cases associated with menstrual cups and intrauterine devices.⁴⁸ Some cases reported in the paediatric literature have raised doubts about the causal relationship between menstrual TSS and tampon usage.^98,99

Table 5: The 2011 centres for disease-control and prevention TSS case definition

Clinical criteria

Fever: ≥ 102.F°

Rash: diffuse macular erythroderma

Desquamation: 1–2 weeks following the appearance of the rash

Hypotension: systolic blood pressure ≤ 90 mm Hg for adults or less than the fifth percentile by age for children aged < 16 years old

Multisystem involvement (three or more of the following organ systems):

Gastrointestinal: vomiting or diarrhoea at the onset of illness

Muscular: severe myalgia or creatine phosphokinase level at least twice the upper limit of normal

Mucous membrane: vaginal, oropharyngeal, or conjunctival hyperaemia

Renal: blood urea nitrogen or creatinine at least twice the upper limit of normal for the laboratory, or urinary sediment with pyuria (greater than or equal to 5 leukocytes per high-power field) in the absence of urinary tract infection

Hepatic: total bilirubin, alanine aminotransferase enzyme, or aspartate aminotransferase enzyme levels at least twice the upper limit of normal laboratory

Hematologic: platelets less than 1,00,000/mm³

Central nervous system: disorientation or alterations in consciousness without focal neurologic signs when fever and hypotension are absent

Laboratory Criteria: Negative results on the following tests, if obtained:

Blood or cerebrospinal fluid cultures: blood culture may be positive for Staphylococcus aureus

Negative serologies for Rocky Mountain spotted fever, leptospirosis, or measles

Probable TSS - Laboratory criteria and four of the five clinical criteria.

Confirmed TSS - Laboratory criteria and all 5 of the clinical criteria, unless the patient dies before desquamation occurs

TSS: Toxic Shock Syndrome

This is corroborated by case studies of adolescents who continued to experience recurring TSS episodes despite discontinuing tampon use.^100,101

TSST-1 adheres to human vaginal epithelial cells, potentially through the CD40 receptor, and in conjunction with cytolysins, triggers the generation of pro-inflammatory chemokines, such as IL-8. This cascade of events ultimately results in the infiltration of cells from both the innate and acquired immune systems into the submucosa, leading to the deterioration and increased permeability of mucous membrane barriers.¹⁰²

Clinically, patients with mTSS typically present with widespread macular erythema that resolves within three days; however, papulopustular and scarlatiniform eruptions are rarely described. Marked oedema of the feet and hands, accompanied by indolent blistering, may also be observed. Generalised erythema of the conjunctiva, oral, oesophageal, bladder, and vaginal mucosa may be present. Later in the second week, most patients develop widespread, pruritic, maculopapular, and sometimes urticarial lesions. Retiform purpura at the peripheries occurs secondary to low platelet count. A highly characteristic finding of mTSS is desquamation, which occurs 10–21 days after the onset of the disease. It may be limited to the fingertips, involve all the plantar and palmar skin.^51.102,103

A clinical assessment should be conducted to locate tampons, which should be removed if found. Comprehensive general supportive interventions are crucial, including fluid resuscitation and ventilatory assistance. The initial treatment of choice involves administering intravenous clindamycin at 600–900 mg three times daily for up to 1-2 weeks based on the patient’s clinical response.⁵¹ A systematic review on Intravenous Immunoglobulin (IVIG) use highlighted the superior efficacy of polyclonal IVIG in treating TSS, with human-derived poly immunoglobulins offering better neutralisation than synthetic or animal-derived alternatives. IVIG works by neutralising superantigens, effectively treating both staphylococcal and streptococcal TSS.¹⁰⁴

Sanitary napkin irritant contact dermatitis occurs secondary to wet local conditions and friction caused by sanitary napkins. It presents as pruritic dermatitis lesions on the vulva and occasionally on the perineal regions.¹⁰⁵ Allergenic fragrances were identified in products such as tampons and sanitary napkins. The well-known skin-sensitising chemicals found to leach from menstrual hygiene products include α-isomethyl ionone, hexyl cinnamaldehyde and heliotropine, and benzyl salicylate.¹⁰⁶ Colophonium in sanitary napkins can also produce vulvar contact dermatitis.¹⁰⁷ Systemic contact dermatitis due to acrylates in the sanitary pads is known to occur.¹⁰⁸ Menstrual hygiene products are known to induce symptoms resembling vulvodynia.¹⁰⁹ A systematic review on menstrual cup usage identified several adverse effects, including discomfort during insertion and removal, vaginal injuries, irritation of the vagina or cervix, allergic contact dermatitis caused by silicone, and the potential risk of TSS.¹⁰⁴

Dermatological disorders associated with menstrual irregularities

A study reported that, compared to paucibacillary leprosy, female patients with multibacillary leprosy had higher rates of post-onset menstrual irregularities and elevated gonadotropic hormone levels.¹¹⁰ MB leprosy is also linked to autoimmunity, with autoantibodies like Anti-Neutrophilic Cytoplasmic Antibodies (ANCA), anti-mitochondrial, and anti-phospholipid antibodies, suggesting immune-mediated ovarian failure.¹¹¹

Systemic lupus erythematosus is associated with a higher prevalence of menstrual irregularities, including amenorrhoea, oligomenorrhoea, and menorrhagia. These disturbances may result from disease activity, systemic inflammation, and the use of immunosuppressive therapies.^112,113

Dermatosurgery and menstruation

Menstrual irregularities have been reported in some patients, especially associated with liposuction in the lower abdomen and upper thigh areas.¹¹⁴ One study reported that the risk of post-inflammatory hyperpigmentation following CO₂ fractionated laser treatment was highest just before or after menstruation, at the end of the luteal phase.¹¹⁵

Drugs and the menstrual cycle

The drugs used by dermatologists that can produce menstrual irregularities have been mentioned in Table 6.^54,55

Table 6: Drugs commonly used by dermatologists that can produce menstrual irregularities

Antiandrogenic effects

Cyproterone acetate

Danazol

Flutamide

Finasteride

Effect on hormones

Tranexamic acid

Oral contraceptives

Immunosuppressants

Systemic corticosteroids

Methotrexate

Cyclophosphamide

Miscellaneous

Griseofulvin

Isotretinoin

Ketoconazole

Spironolactone

Thalidomide

Conclusion

In conclusion, catamenial dermatoses represent a fascinating and clinically significant area of dermatology that warrants greater attention and understanding. By fostering interdisciplinary collaboration and continuing to explore the hormonal underpinnings of these conditions, we can enhance the quality of care for patients experiencing these challenging and often debilitating skin disorders.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

Use of artificial intelligence (AI)-assisted technology for manuscript preparation

The authors confirm that there was no use of artificial intelligence (AI)-assisted technology for assisting in the writing or editing of the manuscript and no images were manipulated using AI.

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Show Sections

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[3] Farage MA, Neill S, MacLean AB. Physiological changes associated with the menstrual cycle: A review. Obstet Gynecol Surv. 2009;64:58-72.
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[4] Muizzuddin N, Marenus KD, Schnittger SF, Sullivan M, Maes DH. Effect of systemic hormonal cyclicity on skin. J Cosmet Sci. 2005;56:311-21.
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[5] Mobasher P, Foulad DP, Raffi J, Zachary C, Fackler N, Zohuri N, et al. Catamenial hyperpigmentation: A review. J Clin Aesthet Dermatol. 2020;13:18-21.
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[6] Pelletier G, Ren L. Localization of sex steroid receptors in human skin. Histol Histopathol. 2004;19:629-36.
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[7] Zachary C, Fackler N, Juhasz M, Pham C, Mesinkovska NA. Catamenial dermatoses associated with autoimmune, inflammatory, and systemic diseases: A systematic review. Int J Womens Dermatol. 2019;5:361-7.
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[8] Gasser S, Heidemeyer K, von Wolff M, Stute P. Impact of progesterone on skin and hair in menopause - a comprehensive review. Climacteric. 2021;24:229-35.
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[9] Kanda N, Watanabe S. Regulatory roles of sex hormones in cutaneous biology and immunology. J Dermatol Sci. 2005;38:1-7.
[CrossRef] [Google Scholar]

[10] Zomer HD, Cooke PS. Targeting estrogen signaling and biosynthesis for aged skin repair. Front Physiol. 2023;14:1281071.
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[11] Thornton MJ. The biological actions of estrogens on skin. Exp Dermatol. 2002;11:487-502.
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[12] Giersch GEW, Morrissey MC, Katch RK, Colburn AT, Sims ST, Stachenfeld NS, et al. Menstrual cycle and thermoregulation during exercise in the heat: A systematic review and meta-analysis. J Sci Med Sport. 2020;23:1134-40.
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[13] Birch MP, Messenger A. ‘Bad hair days’, scalp sebum excretion and the menstrual cycle. J Cosmet Dermatol.. 2003;2:190-4.
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[24] Senila SC, Ungureanu L, Candrea E, Danescu S, Vasilovici A, Cosgarea R, et al. Progesterone hypersensitivity: Case report with favorable evolution. Exp Ther Med. 2019;17:1125-7.
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A narrative review of Catamenial dermatology: A glimpse into the menstrual symphony

Abstract

Keywords

Catamenial

menstruation

progesterone hypersensitivity

autoimmune progesterone dermatitis

menstrual toxic shock syndrome

cutaneous endometriosis.

Introduction

Hormonal changes in the menstrual cycle

Physiological effects on skin and appendages

In skin

Sweat glands

Hair

Nails

Catamenial pigmentary changes

Aberrant skin response to hormones

Autoimmune progesterone dermatitis

Oestrogen dermatitis

Menstruation and sexually transmitted infections

Dermatoses exacerbated with menstruation

Cutaneous endometriosis

Vicarious menstruation

Dermatoses related to the use of menstrual hygiene products

Dermatological disorders associated with menstrual irregularities

Dermatosurgery and menstruation

Drugs and the menstrual cycle

Conclusion

Declaration of patient consent

Financial support and sponsorship

Conflicts of interest

Use of artificial intelligence (AI)-assisted technology for manuscript preparation

References

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